More than 300,000 US war fighters in Operations Iraqi and Enduring Freedom have sustained some form of traumatic brain injury (TBI), caused primarily by exposure to blasts. Many victims are occupants in vehicles that are targets of improvised explosive devices. These underbody blasts expose the occupants to vertical acceleration that can range from several to more than 1,000 G; however, it is unknown if blast-induced acceleration alone, in the absence of exposure to blast waves and in the absence of secondary impacts, can cause even mild TBI.
We approached this knowledge gap using rats secured to a metal platform that is accelerated vertically at either 20 G or 50 G in response to detonation of a small explosive (pentaerythritol tetranitrate) located at precise underbody standoff distances. All rats survived the blasts and were perfusion fixed for brain histology at 4 hours to 30 days later.
Robust silver staining indicative of axonal injury was apparent throughout the internal capsule, corpus callosum, and cerebellum within 24 hours after blast exposure and was sustained for at least 7 days. Astrocyte activation, as measured morphologically with brains immunostained for glial fibrillary acidic protein, was also apparent early after the blast and persisted for at least 30 days.
Exposure of rats to underbody blast-induced accelerations at either 20 G or 50 G results in histopathologic evidence of diffuse axonal injury and astrocyte activation but no significant neuronal death. The significance of these results is that they demonstrate that blast-induced vertical acceleration alone, in the absence of exposure to significant blast pressures, causes mild TBI. This unique animal model of TBI caused by underbody blasts may therefore be useful in understanding the pathophysiology of blast-induced mild TBI and for testing medical and engineering-based approaches toward mitigation.